Human rhinoviruses (HRVs) are the major cause of common cold. Although the majority of HRV infections only cause mild disease, Rhinoviruses can also cause lower respiratory tract infections resulting in severe disease in children, in the elderly and in immunosuppressed patients. Their impact on overall morbidity and their economic cost worldwide are considerable.
Rhinoviruses are small RNA, non-enveloped, viruses belonging to the family picornaviridae. Until now, over 100 serotypes of Rhinoviruses have been identified by specific antisera in a collaborative program supported by the World Health Organization (WHO). Rhinoviruses are divided into major (90%) and minor (10%) groups, according to their cellular receptor usage. An alternative classification, dividing the viruses into group A and B, based on sensitivity to antiviral compounds and correlating with sequence similarities and pathogenicity, has also been proposed[1]. 
In recent years, some researchers have identified new rhinoviruses which cannot be classified into traditional group A or B. McErlean et al[2] screened 1244 nasopharyngeal aspirates collected from patients aged from 1 day to 80 years who presented to Queensland hospitals or general practitioners with symptoms of acute respiratory tract infections during 2003. Among the samples screened, 17 were identified as new rhinovirus positive and the authors named the new rhinovirus as HRV-QPM, which was classified into HRV-A2. The whole genome of HRV-QPM is shorter than all other known HRVs' and isolation of the strain was unsuccessful using human cell lines HeLa-Ohio, A549, MRC-5 and W138. Kistler et al[3] used virochip to test samples from recruited adults who had cold symptoms from the fall of 2001 to December of 2004. They found 5 divergent HRVs named as HRV‘X’, which possessed slightly more sequence similarity to HRV-A than to HRV-B reference serotypes. None of the divergent HRV‘X’ isolates were culturable. Lee et al[4] used Respiratory Multicode Assay to analyze nasal lavage samples of infants. They found 5 distinct strains and proposed that they represent a new HRV genetic group (HRV-C). None of the samples containing the new HRV strains produced cytopathic effect (CPE) in standard WI-38 or MRC-5 cell cultures used for the detection and isolation of HRV. Using RT-PCR method, Lau et al[5] screened 200 Nasopharyngeal Aspirates (NPAs) collected from hospitalized children during a 1-year period (November 2004 to October 2005). They found 21 positive for HRV which belonged to a distinct genetic cluster, i.e., clade C, with nucleotide identity of <63% to known HRV-A strains and nucleotide identity of <61% to known HRV-B strains. Renwick et al[6] used MassTag PCR to investigate 97 nasopharyngeal aspirates from children hospitals during the interval of 2003-2006. They found 30 HRV sequences which did not match with known HRVA, HRVB, or Human Enterovirus (HEV) sequences.